SPECIALTY UPDATE
ARTICLE 3
ORAL AND MAXILLOFACIAL SURGERY




































































































Antiplatelet therapy and exodontia
Willem H. Schreuder, DMD, MD; Zachary S. Peacock, DMD,
MD, FACS
I
n general, dentists can complete exodontia for
patients taking antiplatelet therapy without the
occurrence of bleeding sequelae.1 Local hemostatic
measures are effective in limiting intra- and post-
operative bleeding with continuation of antiplatelet
medications. For each case that involves deciding
whether to alter antiplatelet regimens, the dentist must
compare the patient’s risk of experiencing perioperative
hemorrhage with that of a thromboembolic event.
Alteration of therapy always requires the dentist to
consult with the patient’s prescribing physician.
MANAGEMENT CONSIDERATIONS
In this review, we will describe the indications for and
the mechanisms of antiplatelet therapy in the context
of perioperative management of patients requiring exo-
dontia or other dentoalveolar surgery. When assessing
a patient on antiplatelet therapy, the dental practitioner
must weigh the patient’s risk of experiencing early and
late postoperative bleeding against the risk of experi-
encing thromboembolic events with discontinuation of
therapy. Dental practitioners should take note of the
following management considerations:
- The dental practitioner must consider the patient’s
complete medical history and all comorbidities, includ-
ing the indications for antiplatelet therapy and the time
This article has an accompanying online continuing education activity
available at: http://jada.ada.org/ce/home.
Copyright ª 2015 American Dental Association. All rights reserved.
ABSTRACT
Background. This is a review of the management
considerations regarding exodontia for patients taking
antithrombotic medications that affect platelet function
or aggregation.
Methods. The authors reviewed the literature, focusing
on the indications and mechanisms of antiplatelet therapy
and the perioperative management of patients taking
these agents who require exodontia or other dentoal-
veolar surgery.
Results. Dentists making management decisions
regarding patients taking antiplatelet therapy should
consider the patient’s risk of experiencing perioperative
hemorrhage against the risk of experiencing complica-
tions associated with thromboembolic events. The risk of
perioperative bleeding complications is low for patients
taking single or dual antiplatelet therapy. Intraoperative
and postoperative bleeding can be controlled with local
hemostatic measures.
Conclusion. For patients taking antiplatelet medication,
bleeding risk for exodontia is generally lower than the risk
of experiencing thromboembolic events owing to cessa-
tion of therapy.
Practical Implications. Dentists can safely complete
exodontia in patients who continue taking antiplatelet
therapy. The dentist should consult the patient’s pre-
scribing physician before considering altering the pa-
tient’s antiplatelet therapy regimen.
Key Words. Tooth extraction; exodontia; antiplatelet;
aspirin; NSAID; thienopyridine; clopidogrel; dipyr-
idamole; postoperative bleeding.
JADA 2015:146(11):851-856
http://dx.doi.org/10.1016/j.adaj.2015.04.024
JADA 146(11) http://jada.ada.org November 2015 851
 SPECIALTY UPDATE
since the event or intervention that prompted the patient
to start antiplatelet therapy.
- Whenever possible, the dental practitioner should
maintain the patient’s intake of aspirin and other anti-
platelet therapies, including dual antiplatelet therapy.
- The dental practitioner should not interrupt the pa-
tient’s dual antiplatelet therapy until at least 12 months
after placement of a coronary stent. The practitioner
should not perform elective procedures requiring alter-
ation of therapy during this time.
- The dental practitioner must consider the extent
of the procedure and local factors involved when de-
termining a patient’s risk of bleeding. Extraction of
multiple teeth with existing inflammation (that is, peri-
odontal disease) may increase the risk of experiencing
perioperative bleeding.
- The practitioner can aid local hemostasis at the time
of extraction and in the event of postoperative bleeding
with the use of sutures, gelatin (for example, Gelfoam
[Pfizer]), cellulose (for example, Surgicel [Ethicon]), and
application of continuous pressure with gauze. The use
of local anesthetic with vasoconstrictor decreases peri-
and postoperative blood loss.2 Caution must be used in
patients with a history of cardiac ischemia.3
- Special considerations for procedures that are asso-
ciated with an elevated risk of bleeding (for example, full-
mouth extractions in patients taking dual antiplatelet
therapy) include completing the extractions in stages,
scheduling the procedure early in the day and week
to allow time to manage bleeding, or considering the
alteration of the patient’s antiplatelet therapy.
- The practitioner should address questions regard-
ing antiplatelet therapy with the patient’s prescribing
physician.
BACKGROUND AND DISCUSSION
An increasing number of anticoagulant medications
are being prescribed for patients with cardiovascular
comorbidities. Performing invasive dental procedures in
patients who are taking anticoagulants requires knowl-
edge of normal hemostasis and the various ways it can
be inhibited.
Antithrombotic medications include inhibitors of
platelet function and aggregation (for example, aspirin)
as well as those that inhibit the coagulation cascade (for
example, warfarin). Generally, antiplatelet agents are
prescribed for the purpose of primary and secondary
prevention of acute ischemic cerebrovascular and car-
diovascular events.4,5 Guidelines also recommend the use
of antiplatelet agents for patients with occlusive peripheral
vascular disease and to prevent thrombosis after the im-
plantation of bare metal or drug-eluting stents (DES).6,7
The risk of intra- and postoperative bleeding is
increased in the presence of platelet inhibition.8 Dentists
are confronted routinely with the dilemma of whether
to request that patients modify or discontinue the use
852 JADA 146(11) http://jada.ada.org November 2015
of these agents before having invasive dental treatment.
Dentists always must consider the indication for anti-
platelet medications and the patient’s underlying medical
conditions.
Normal hemostasis. The physiologic mechanism of
hemostasis occurs to prevent extravasation of blood in
the event of blood vessel injury. The coagulation process
is divided into 3 distinct, interrelated phases9: primary
hemostasis (the formation of a platelet aggregate), sec-
ondary hemostasis (the formation of a fibrin clot by
activating coagulation factors), and fibrinolysis (the
breakdown of the clot after tissue and vascular repair).
Disruption of the endothelial lining of a blood vessel
leads to platelet binding (via the von Willebrand factor)
to proteins of the subendothelial matrix (that is, platelet
adhesion).10,11 Platelets change in shape as the coagula-
tion process becomes activated further and bind to other
platelets via another membrane integrin, glycoprotein
(GP) IIb-IIIa during platelet aggregation.10 Platelet acti-
vation results in exocytosis of dense and alpha granules
containing adenosine diphosphate (ADP), thromboxane
A2, epinephrine, and thrombin, which promotes further
activation and aggregation.9
The primary clot consists of a fibrin mesh containing
the platelet aggregate, together with entrapped red and
white blood cells. The formation of fibrin starts early
during platelet activation.12 The coagulation cascade re-
sults from a complex interaction of clotting factors as
well as cellular surfaces producing a fibrin clot.12
Antiplatelet medications. Increased platelet activity
also is implicated in pathologic thrombosis, atheroscle-
rosis, and coronary artery disease. This has led to the
development of various classes of antiplatelet medica-
tions (Figure).
Acetylsalicylic acid (aspirin) irreversibly inactivates
the enzyme cyclo-oxygenase (COX) type 1, through
selective acetylation.13 The enzyme is responsible for
the formation of prostaglandins and thromboxane A2,
which are critical to platelet activation and aggregation.13
Nonsteroidal anti-inflammatory drugs (NSAIDs) revers-
ibly inactivate the COX pathway, with their effect on
platelet function dependent on plasma half-life.14 COX
type 2 selective inhibitors (for example, celecoxib) have
less effect on primary hemostasis.15
Thienopyridines (for example, clopidogrel, ticlopidine,
prasugrel) selectively and irreversibly inhibit the platelet
ADP receptor (P2Y12 receptor).16 The most common,
clopidogrel (Plavix [Bristol-Myers Squibb/Sanofi Phar-
maceuticals Partnership]), affects the ADP-dependent
activation of the GP IIb-IIIa complex in platelet
ABBREVIATION KEY. ADP: Adenosine diphosphate.
COX: Cyclo-oxygenase. DES: Drug-eluting stent. GP:
Glycoprotein. NSAID: Nonsteroidal anti-inflammatory drugs.
TxA2: Thromboxane A2.
 SPECIALTY UPDATE
ADP
Dipyridamole
ADP
Thrombin
Collagen PLATELET ACTIVATION
TxA2
COX-1
TxA2
Figure. Platelet activation occurs with binding of adenosine diphosphate (ADP) to the ADP (P2Y12) receptor. Thienopyridines (clopidogrel, ticlopidine,
and prasugrel) selectively and irreversibly inhibit the platelet ADP receptor. Glycoprotein (GP) IIb-IIIa (which is an integrin receptor for fibrinogen and
von Willebrand factor) inhibitors block platelet aggregation, whereas aspirin inhibits cyclo-oxygenase (COX) that blocks the formation of thomboxane
A2 (TxA2), which is also critical to activation. COX-1: Cyclo-oxygenase type 1.
aggregation.16 Typically, clopidogrel is combined with
aspirin. Investigators have shown that this dual anti-
platelet therapy has been effective in the medical man-
agement of acute coronary syndrome17,18 and after
coronary artery stenting.19,20 The newer generation of
P2Y12 inhibitors, including prasugrel and ticagrelor, is
more potent, and exhibit less pharmacologic variability
than does clopidogrel.16
Dipyridamole (Persantine [Boehringer Ingelheim
Pharmaceuticals]) disrupts platelet aggregation by
inhibiting phosphodiesterases, resulting in increased
levels of platelet cyclic adenosine monophosphate and
cyclic guanosine monophosphate, which block the
platelet response to various stimuli such as ADP.13,21
It also leads to the disruption of platelet aggregation
and vasodilation by blocking the reuptake of adenosine
into platelets, endothelial cells, and erythrocytes.13,21
It is effective in combination with aspirin for treating
ischemic stroke and transient ischemic attacks.21
GP IIb-IIIa inhibitors are an additional class of anti-
platelet agents given intravenously during percutaneous
coronary intervention (that is, angioplasty with or
without stent implantation) to treat acute myocardial
infarction.22 They prevent binding to the GP IIb-IIIa
receptor on the platelet membrane, preventing aggrega-
tion. Dentists are unlikely to encounter patients taking
these medications as these drugs are not given orally or
to outpatients.
Clopidogrel
Ticlopidine
Prasugrel
ADP P2Y12
PLATELET AGGREGATION
GP IIb-IIIa
receptor
Fibrinogen
Abciximab
Eptifibatide
Tirofiban
Aspirin
Risk of interrupting antiplatelet therapy. Having
patients discontinue the use of any antiplatelet therapies
before undergoing invasive dental procedures remains
common practice. Clinicians often overestimate the
patient’s risk of experiencing severe bleeding with exo-
dontia; this overestimation may be based on reports
of increased bleeding in patients taking antiplatelet
medications after general and gynecological surgical
procedures.23 Withdrawing antiplatelet medication,
however, increases the patient’s risk of experiencing
thrombosis and, potentially, myocardial infarction,
stent occlusion, and cerebrovascular accidents.24-28
Interrupting the use of chronic aspirin therapy may lead
to a period of rebound hypercoagulability and increased
thromboembolic complications.29
After coronary stent implantation, the patient must
follow a dual antiplatelet therapy regimen with aspirin
and a thienopyridine (for example, clopidogrel) until
the stents are fully re-endothelialized (that is, 3 months
for bare metal stents and at least 7 months for DES).30
Guidelines recommend that patients receive at least
12 months of dual antiplatelet therapy after the implan-
tation of either type of stent.25,31,32 Premature discontin-
uation of thienopyridine therapy is associated with
a marked increase in the risk of experiencing stent
thrombosis.24-26 Dental practitioners should defer any
surgical procedures requiring alteration of the patient’s
therapy for a minimum of 6 weeks after a patient has
JADA 146(11) http://jada.ada.org November 2015 853
 SPECIALTY UPDATE
received a bare metal stent and for 6 months after a
DES.33 Dental practitioners should defer a patient’s
elective dental extractions that require an alteration in
therapy for at least 12 months after stent placement.25,31,32
For decisions regarding antiplatelet medications,
dentists must consider not only the patient’s risk of
experiencing perioperative hemorrhage or thrombo-
embolic events, but also the consequences of the
occurrence of these complications. Thromboembolic
events may lead to permanent disability or death,
whereas bleeding complications typically are only in-
convenient to the patient or provider. Burger and
colleagues8 recommended discontinuing antiplatelet
therapy only if the consequence of hemorrhage would
be expected to be similar or more severe than the
observed cardiovascular risks. Exodontia would not meet
this criterion.
Risk of bleeding after exodontia. No reliable method
exists to predict accurately the likelihood of a patient
having postoperative bleeding after undergoing an oral
surgical procedure while continuing antiplatelet medi-
cations.34 Brennan and colleagues35 found no correlation
between cutaneous bleeding time and oral bleeding time
in patients following antiplatelet regimens.
Napenas and colleagues36 retrospectively assessed
bleeding events for patients on single nonaspirin or dual
antiplatelet therapy who required invasive dental treat-
ment (including exodontia). Although hemostatic mea-
sures (for example, sutures, gelatin sponge) were used
in only 59%, none of the 43 included participants had
prolonged bleeding. The investigators concluded that the
risk of experiencing perioperative bleeding complica-
tions was low for patients taking single or dual anti-
platelet therapy. Madan and colleagues37 performed
a prospective cohort study (n ¼ 51) and reported no
postoperative bleeding episodes in paticipants taking
aspirin (75-100 milligrams per day). Only one case
required intraoperative packing of hemostatic agents
to achieve hemostasis.
Studies comparing discontinuation versus contin-
uation of aspirin therapy and NSAIDs have also
shown little difference in bleeding after exodontia.38-42
The investigators of a randomized controlled trial of
36 patients who were receiving either a high-dose
aspirin (325 mg/day) or a placebo for 2 days before and
after the extraction concluded that there was no dif-
ference in patients’ bleeding episodes and no indica-
tion for discontinuing aspirin for invasive dental
procedures.38 Ardekian and colleagues28 randomized
39 study participants to discontinue or continue taking
aspirin (100 mg/day) 7 days before undergoing exo-
dontia, and they found no episodes of uncontrolled
intraoperative or postoperative bleeding. Similarly,
Medeiros and colleagues39 showed in the results of a
randomized study (n ¼ 63) that continuing to take
aspirin (100 mg/day) did not increase blood loss after
854 JADA 146(11) http://jada.ada.org November 2015
surgical extractions of molar teeth when local hemo-
static methods were used.
Considering dual antiplatelet therapy, Lillis and col-
leagues43 reported the results of a prospective study on
postextraction bleeding in patients receiving uninterrupted
nonaspirin (n ¼ 36), aspirin (n ¼ 42), or dual antiplatelet
therapy (n ¼ 33) compared with control participants who
were not taking antiplatelet therapy (n ¼ 532). They re-
ported no postoperative bleeding events. Those receiving
uninterrupted dual antiplatelet therapy had more intra-
operative bleeding than the participants in the other
groups, but the bleeding was managed successfully with
cellulose, sutures, and pressure using gauze.43 Park and
colleagues44 also concluded that dental extractions can be
performed safely in patients continuing combined anti-
platelet regimens with the proper application of pressure
using gauze. The results of their prospective cohort study of
patients receiving dual or triple antiplatelet therapy (n ¼
100) showed no significant difference in intraoperative
blood loss or postoperative bleeding complications
compared with matched controls.44 Accordingly, Bajkin
and colleagues45 concluded that simple tooth extraction
can be performed safely without interrupting the use of
single or dual antiplatelet therapy using only local hemo-
static measures. Olmos-Carrasco and colleagues46 pro-
spectively assessed the presence of bleeding at various
times after extractions in 181 patients on dual antiplatelet
therapy at 11 institutions. Despite a lack of vasocontrictors
or suturing of the extraction site, the investigators found
that intraoperative hemorrhage lasted fewer than 30 mi-
nutes in 91.2% of the study participants. They noted an
absence of any bleeding at 24 hours and at 10 days after
extraction in 89.5% and 96.1% of patients, respectively. The
study participants’ risk of bleeding for more than 30 mi-
nutes was increased in the presence of inflammation and
after the extraction of 3-rooted teeth.
Although fewer data exist assessing new antiplatelet
agents compared with aspirin, investigators have re-
ported that the risk of bleeding complications during and
after exodontia also appears to be low.45,47
CONCLUSION
The risk of adverse cardiovascular events related to dis-
continuing anti-platelet therapy generally outweighs the
risk of increased bleeding during and after exodontia. n
Dr. Schreuder is a research fellow, Department of Oral and Maxillofacial
Surgery, Massachusetts General Hospital and Harvard School of Dental
Medicine, Boston, MA.
Dr. Peacock is an assistant professor, Department of Oral and Maxillo-
facial Surgery, Massachusetts General Hospital and Harvard School of
Dental Medicine, 55 Fruit St., Warren 1201, Boston, MA 02114, e-mail
zpeacock@partners.org. Address correspondence to Dr. Peacock.
Disclosure. Drs. Schreuder and Peacock did not report any disclosures.
Oral and Maxillofacial Surgery is published in collaboration with the
American Association of Oral and Maxillofacial Surgeons.
 SPECIALTY UPDATE
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